Loss of Muscle MTCH2 Increases Whole-Body Energy Utilization and Protects from Diet-Induced Obesity

Liat Buzaglo-Azriel, Yael Kuperman, Michael Tsoory, Yehudit Zaltsman, Liat Shachnai, Smadar Levin-Zaidman, Elad Bassat, Inbal Michailovici, Alona Sarver, Eldad Tzahor, Michal Haran, Cecile Vernochet, Atan Gross

Research output: Contribution to journalArticlepeer-review

Abstract

Mitochondrial carrier homolog 2 (MTCH2) is a repressor of mitochondrial oxidative phosphorylation (OXPHOS), and its locus is associated with increased BMI in humans. Here, we demonstrate that mice deficient in muscle MTCH2 are protected from diet-induced obesity and hyperinsulinemia and that they demonstrate increased energy expenditure. Deletion of muscle MTCH2 also increases mitochondrial OXPHOS and mass, triggers conversion from glycolytic to oxidative fibers, increases capacity for endurance exercise, and increases heart function. Moreover, metabolic profiling of mice deficient in muscle MTCH2 reveals a preference for carbohydrate utilization and an increase in mitochondria and glycolytic flux in muscles. Thus, MTCH2 is a critical player in muscle biology, modulating metabolism and mitochondria mass as well as impacting whole-body energy homeostasis.

Original languageEnglish
Pages (from-to)1602-1610
Number of pages9
JournalCell Reports
Volume14
Issue number7
DOIs
StatePublished - 23 Feb 2016

All Science Journal Classification (ASJC) codes

  • General Biochemistry,Genetics and Molecular Biology

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